The proposed working hypothesis is based on the assumption that the number of adrenergic nerve endings declines with age. Prolonged partial or complete deprivation of the arterial wall of normal sympathetic nervous stimuli leads to degenerative changes in structure and function of the bacterial wall. These disturbances may then be exacerbated by the concurrent hypersensitivity to blood-borne catecholamines. It is postulated that the net effect of these derangements is to predispose the vessel wall even to stresses which are normally well tolerated. The proposed hypothesis will be tested by analysis of specific aspects of lipids biochemistry and histology of the arterial wall under different conditions of sympathetic innervation in combination with additional metabolic interventions. If the proposed concept proves to be valid, new avenues will open for studies in the vessel wall pathophysiology.